ライフサイエンスコーパス: great vessel

1 the antibodies in the blood pools (heart and great vessels).

2 ctopic calcification within the walls of the great vessels.

3 are required for remodeling of the heart and great vessels.

4 truncus arteriosus and abnormalities of the great vessels.

5 s to direct blood flow through the heart and great vessels.

6 the formation of the mature aortic arch and great vessels.

7 eate casts of blood flow of the chambers and great vessels.

8 o avoid laparotomy and cross-clamping of the great vessels.

9 en to the innermost endothelial cells of the great vessels.

10 utermost, adventitial cell population in the great vessels.

11 nexpected plasticity in the formation of the great vessels.

12 dventitial cell population of the developing great vessels.

13 rolling chronic inflammatory diseases of the great vessels.

14 a function of blood volume in the heart and great vessels.

15 Six needles (5.2%) were placed into the great vessels.

16 he immune system, and chronic disease of the great vessels.

17 measurements of blood flow in the heart and great vessels.

18 as, and structural diseases of the heart and great vessels.

19 ation in disorders of the heart and adjacent great vessels.

20 oblique sinuses and around the roots of the great vessels.

21 icular septal defect, 4 transposition of the great vessels, 3 patient ductus arteriosus, 3 partial an

22 ildren and can be used to delineate abnormal great vessel anatomy.

23 ith a constellation of heart, outflow tract, great vessel and pharyngeal gland defects that phenocopi

24 ing thoracic aorta, such as proximity to the great vessels and arch tortuosity, have been and remain

25 nomalous coronary artery with respect to the great vessels and cardiac chambers.

26 lular matrix protein abundantly expressed in great vessels and cardiac valves during embryogenesis, a

27 Transposition of the great vessels and common ventricle had higher rates of n

28 r, with higher rates of transposition of the great vessels and common ventricle patients compared wit

29 Significant constriction of the great vessels and ductus arteriosus was observed with L-

30 ter-generated three-dimensional image of the great vessels and ductus arteriosus.

31 malformations of the cardiac outflow tract, great vessels and heart due, at least in part, to failur

32 e are extensive defects in remodeling of the great vessels and heart resulting in death at ~E14.5.

33 are essential for normal development of the great vessels and the heart, giving rise to a range of c

34 nary veins, scattered within the wall of the great vessels, and a strictly delimited cluster between

35 allot, Ebstein anomaly, transposition of the great vessels, and common ventricle) and (2) patients <2

36 In addition to information about the heart, great vessels, and coronary arteries, these examinations

37 We find that the great vessels are strikingly dilated and frequently deve

38 Great vessel areas correlated well with body surface are

39 ac magnetic resonance reference Z scores for great vessel areas in normal children and adolescents in

40 ignificant variations in the whole heart and great vessel, automatic CHD segmentation using CT images

41 maging (ventricular volumes and function and great vessel blood flow) and hemodynamic assessment (inv

42 ng the function and anatomy of the heart and great vessels, but its emerging role as one of the domin

43 lood vessels, nor by defects in the heart or great vessels, but were due to abnormal development of t

44 agangliomas are typically located around the great vessels, coronary arteries (atrioventricular groov

45 uses a variety of pharyngeal arch artery and great vessel defects, as well as malformations in many o

46 The malalignment of the great vessels described in this animal model are similar

47 uency of vessel defects scored at the end of great vessel development.

48 enital heart disease, but normative data for great vessel dimensions in pediatric subjects are scarce

49 is in native (2C) or mechanical valves (1B), great vessel disease and injury (2C), penetrating chest

50 In the cardiac outflow tract and great vessels, ET(A)(-/-) cells are excluded from the wa

51 In all patients, ventricular volumes and great vessel flow were measured.

52 arctation of the aorta, transposition of the great vessels, hypoplastic left heart syndrome, oral cle

53 tricuspid atresia with transposition of the great vessels in 4, and other diagnoses in 3.

54 onship between the coronary arteries and the great vessels in subjects with normal cardiac morphology

55 The ductus differs primarily from the great vessels in that it is a muscular rather than an el

56 c neural crest in formation of the heart and great vessels in the mouse and, furthermore, shows that

57 to the blood pool, visible as the heart and great vessels in the trunk and limbs, plus diffuse signa

58 Congenital lesions of the great vessels, including the aorta, pulmonary arteries,

59 dibulum (OFT myocardial remnant) beneath the great vessels, indicating failure of OFT shortening.

60 fined as pneumothorax, hemothorax, aortic or great vessel injury, 2 or more rib fractures, ruptured d

61 metric embryonic aortic arches to the mature great vessels is a complex morphogenetic process, requir

62 ascular smooth muscle differentiation in the great vessels is disrupted.

63 malities eventually lead to various types of great vessel malformations highly similar to those seen

64 ithin the DGS phenotypic spectrum, including great vessel malformations, hypoplastic pulmonary and ao

65 E axis signaling in the vulnerable heart and great vessels may be essential in controlling and preven

66 ly with respect to assessment of cardiac and great vessel morphology and left ventricular function.

67 ammation (n = 4), blood pool activity in the great vessels (n = 2), bowel uptake (n = 1) and unknown

68 enzyme, ECE-1, in the pharyngeal arches and great vessels of the developing chick embryo.

69 lood flow patterns in the heart and adjacent great vessels, offering detailed insights into their com

70 congenitally corrected transposition of the great vessels often reach childbearing age.

71 nding to multimodal stressors applied to the great vessels or heart.

72 s that result from abnormal septation of the great vessels' outflow tracts.

73 umental in diagnosing cardiac and associated great vessel pathology and in identifying structural abn

74 e studies assign the embryonic origin of the great vessel progenitors to the interface between the ph

75 framework combining both the whole heart and great vessel segmentation in complex CHD.

76 ed with the state-of-the-art whole heart and great vessel segmentation method in normal anatomy.

77 eal arches, from which many craniofacial and great vessel structures arise.

78 s, as well as defects in cardiac outflow and great vessel structures, which are derived from cephalic

79 es are vital for the development of a mature great vessel system.

80 FT cardiomyocytes by PCD is required for the great vessels to make their proper connections with the

81 e instances, the infundibulum connected both great vessels to the right ventricle in a side-by-side a

82 re injuries in children, such as cardiac and great vessel trauma, may remain undiagnosed precisely be

83 ssures and samples from cardiac chambers and great vessels using antegrade, transseptal, and retrogra

84 s, eg, neural tube defects, transposition of great vessels, ventricular septal defect, atrial septal

85 Associated deformity of the trachea or great vessels was recorded as absent or present.

86 congenitally corrected transposition of the great vessels was studied in 22 women.

87 2 patients (50%), and d-transposition of the great vessels was the diagnosis for 4 patients (16%).

88 images, and through-plane flow images of the great vessels were acquired.

89 ded surface display images of the airway and great vessels were generated from volumetric CT data and

90 congenitally corrected transposition of the great vessels were identified.

91 artery and its course in relationship to the great vessels were unequivocally demonstrated.

92 nary patterns, both of which loop around the great vessels, were associated with significant mortalit

93 ressed in neural crest, developing heart and great vessels, whereas Ahdc1 is not.

94 %-58%) and proximity to the aortic valve and great vessels (with potential for dissection complicatio

95 heter management of major CHD lesions of the great vessels, with a focus on coarctation of the aorta,